ReviewCancers2018
New Insights into Protein Kinase B/Akt Signaling: Role of Localized Akt Activation and Compartment-Specific Target Proteins for the Cellular Radiation Response.
Review in Cancers, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
67 citing papers in PubMed, 1 synthesis or guideline pooled it, 127 citations in OpenAlex.
- The effects of flavonoid baicalein on miRNA expressions in cancer: a systematic review.Naunyn-Schmiedeberg's archives of pharmacology · 2025Pooled it
- Expression of HGF, pMet, and pAkt is related to benefit of radiotherapy after breast-conserving surgery: a long-term follow-up of the SweBCG91-RT randomised trial.Molecular oncology · 2020Trial
- Ibrutinib therapy downregulates AID enzyme and proliferative fractions in chronic lymphocytic leukemia.Blood · 2019Trial
- Colitis-associated colorectal carcinogenesis: molecular mechanisms and therapeutic potential.Molecular biomedicine · 2026Review
- Urolithin A blocks colorectal cancer progression by AKT1 inhibition-driven immune activation.Scientific reports · 2026Article
- A Novel Role for the Small Molecule Cinnamaldehyde in Protecting AgainstAntioxidants (Basel, Switzerland) · 2026Article
- Review
- Hallachrome, a marine anthraquinone, impairs cell proliferation by acting as a functional mitochondrial uncoupler in A375 melanoma cells.Frontiers in pharmacology · 2026Article
- Uracil derivatives/ursolic acid hybrids - naturally derived compounds as anticancer agents.Scientific reports · 2025Article
- HER2-Positive Breast Cancer-Current Treatment Management and New Therapeutic Methods for Brain Metastasis.Biomedicines · 2025Review
- Targeting HSP90 in Gynecologic Cancer: Molecular Mechanisms and Therapeutic Approaches.Cell biochemistry and biophysics · 2025Review
- Preeclampsia as a Study Model for Aging: The Klotho Gene Paradigm.International journal of molecular sciences · 2025Review
- Review
- Microglia-induced neuroinflammation in hippocampal neurogenesis following traumatic brain injury.Heliyon · 2024Review
- The ability of microRNAs to regulate the immune response in ischemia/reperfusion inflammatory pathways.Genes and immunity · 2024Review
- Selectivity Studies and Free Energy Calculations of AKT Inhibitors.Molecules (Basel, Switzerland) · 2024Article
- Signaling pathways that activate hepatic stellate cells during liver fibrosis.Frontiers in medicine · 2024Review
- Multiple endocrine neoplasia type 4 (MEN4): a thorough update on the latest and least known men syndrome.Endocrine · 2023Review
- Unlocking New Avenues in Breast Cancer Treatment: The Synergy of Kinase Inhibitors and Immunotherapy.Cancers · 2023Review
- MicroRNA based combinatorial therapy against TKIs resistant CML by inactivating the PI3K/Akt/mTOR pathway: a review.Medical oncology (Northwood, London, England) · 2023Review
7 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Genetic alterations driving aberrant activation of the survival kinase Protein Kinase B (Akt) are observed with high frequency during malignant transformation and cancer progression. Oncogenic gene mutations coding for the upstream regulators or Akt, e.g., growth factor receptors, RAS and phosphatidylinositol-3-kinase (PI3K), or for one of the three Akt isoforms as well as loss of the tumor suppressor Phosphatase and Tensin Homolog on Chromosome Ten (PTEN) lead to constitutive activation of Akt. By activating Akt, these genetic alterations not only promote growth, proliferation and malignant behavior of cancer cells by phosphorylation of various downstream signaling molecules and signaling nodes but can also contribute to chemo- and radioresistance in many types of tumors. Here we review current knowledge on the mechanisms dictating Akt's activation and target selection including the involvement of miRNAs and with focus on compartmentalization of the signaling network. Moreover, we discuss recent advances in the cross-talk with DNA damage response highlighting nuclear Akt target proteins with potential involvement in the regulation of DNA double strand break repair.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.